Mehrdad Arjomandi, MD
|School||UCSF School of Medicine|
|Address||4150 Clement Street|
San Francisco CA 94121
Dr. Arjomandi is Associate Professor of Medicine in the Division of Pulmonary, Critical Care, Allergy, Immunology, and Sleep Medicine at UCSF with a joint appointment at San Francisco Veterans Affairs Medical Center. He is Associate Director of the UCSF Human Exposure Laboratory at San Francisco General Hospital, and an investigator at the UCSF Center for Tobacco Control Research and Education.
Dr. Arjomandi received his bachelor degree in molecular biology from University of California San Diego in 1991, and his MD degree from Stanford University School of Medicine in 1996. He completed his residency in Internal Medicine at UCLA Medical Center (1999) and his fellowship in Pulmonary and Critical Care Medicine at UCSF (2003). Dr. Arjomandi’s current funding include NIH/NHLBI Mentored Patient- oriented Career Development Award (K23), the UCSF Flight Attendants Medical Research Institute (FAMRI) Center of Excellence Research Award, and the Health Effect Institute (HEI).
The lung is constantly exposed to various environmental pollutants, allergens, and toxins, which interact with airways and alveoli and result in inflammation, injury, and disease. Exposure-related pulmonary diseases are increasingly recognized as a growing global problem. Although exposures to various environmental agents cause a range of airway and lung diseases, evidence exists to suggest that many of these agents share common pathways of inflammation and injury. Oxidative stress has been recognized as such a common underlying mechanism that contributes to pathophysiology of many exposure-related lung diseases.
My laboratory primary research interest is to study the role of oxidative stress in pathogenesis of lung diseases. We have focused our effort on studying the physiology as well as inflammatory mechanisms through which exposure to pollutants and oxidative stress contributes to lung diseases:
1- Oxidative Stress and Innate Immunity: We study how oxidative stress modulates innate immune responses in various exposure-response models such as ozone-induced, allergen-induced, and wood or tobacco smoke-induced oxidative stress and airway inflammation. We study these effects through controlled human exposure studies, and evaluation of in vivo and ex vivo responses of airway inflammatory cells (alveolar macrophages) and bronchial epithelial cells.
2- Early Physiologic, anatomic, and inflammatory changes in COPD: We study the physiologic, anatomic, and inflammatory changes in a well-characterized cohort of subjects with long and remote history of intense exposure to secondhand tobacco smoke who have evidence of mild COPD. We characterize our cohort by exercise physiology, quantitative radiographic imaging of lungs, and assessment of airway inflammation and lung tissue matrix degradation.
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